Window Of Opportunity For Sustainable Energy

The article considers the ways of increasing the sustainability of the energy sector in an unstable environment and technology modernization that implies radical structural transformations in the configuration of energy systems. The authors show that power engineering should be given a special emphasis in this context because it is the most stable branch of the energy sector in terms of its vulnerability to crisis. The article suggests that the processes of electrification that further technological progress and increase the innovative potential of a region’s economy should be viewed as a driver forging a ‘smart partnership’ of power engineering and manufacturing. The authors analyze positive effects and price risks that emerge in the course of the implementation of electrification programs and use the analysis as a basis for their recommendations for developing regional electric power systems and effective relationships between utilities and consumers.The work was supported by Act 211 Government of the Russian Federation, contract № 02.A03.21.0006

Interdisciplinarity as heuristic resource for energy management

As high-tech industries continue to experience dynamic growth and problems of development in high-tech industries are getting increasingly complex, managers have to embrace the need for new competencies that match present-day challenges. This calls for a qualitative change in the architecture of education to bring it up to date with contemporary trends. Using cases from Russia, the paper aims to provide a groundwork for an interdisciplinary approach to building professional competencies in energy managers as a framework for forward-looking management of high-tech industries in a nonlinear environment. The authors identify factors that determine the new management imperative and set out methodological principles of developing a management culture. A model of professionalism in management is proposed that is the result of a complex interplay of interrelated competencies. The paper also explains the key features of an interdisciplinary training programme. To prove the research hypothesis, an analysis was conducted of empirical data from expert reviews by executives at Russian energy companies and leading academics

Neural connectivity in syntactic movement processing

Linguistic theory suggests non-canonical sentences subvert the dominant agent-verb-theme order in English via displacement of sentence constituents to argument (NP-movement) or non-argument positions (wh-movement). Both processes have been associated with the left inferior frontal gyrus and posterior superior temporal gyrus, but differences in neural activity and connectivity between movement types have not been investigated. In the current study, functional magnetic resonance imaging data were acquired from 21 adult participants during an auditory sentence-picture verification task using passive and active sentences contrasted to isolate NP-movement, and object- and subject-cleft sentences contrasted to isolate wh-movement. Then, functional magnetic resonance imaging data from regions common to both movement types were entered into a dynamic causal modeling analysis to examine effective connectivity for wh-movement and NP-movement. Results showed greater left inferior frontal gyrus activation for Wh > NP-movement, but no activation for NP > Wh-movement. Both types of movement elicited activity in the opercular part of the left inferior frontal gyrus, left posterior superior temporal gyrus, and left medial superior frontal gyrus. The dynamic causal modeling analyses indicated that neither movement type significantly modulated the connection from the left inferior frontal gyrus to the left posterior superior temporal gyrus, nor vice-versa, suggesting no connectivity differences between wh- and NP-movement. These findings support the idea that increased complexity of wh-structures, compared to sentences with NP-movement, requires greater engagement of cognitive resources via increased neural activity in the left inferior frontal gyrus, but both movement types engage similar neural networks.This work was supported by the NIH-NIDCD, Clinical Research Center Grant, P50DC012283 (PI: CT), and the Graduate Research Grant and School of Communication Graduate Ignition Grant from Northwestern University (awarded to EE). (P50DC012283 - NIH-NIDCD, Clinical Research Center Grant; Graduate Research Grant and School of Communication Graduate Ignition Grant from Northwestern University)Published versio

Association Between Blood Pressure and Adverse Renal Events in Type 1 Diabetes.

ObjectiveTo compare different blood pressure (BP) levels in their association with the risk of renal outcomes in type 1 diabetes and to determine whether an intensive glycemic control strategy modifies this association.Research design and methodsWe included 1,441 participants with type 1 diabetes between the ages of 13 and 39 years who had previously been randomized to receive intensive versus conventional glycemic control in the Diabetes Control and Complications Trial (DCCT). The exposures of interest were time-updated systolic BP (SBP) and diastolic BP (DBP) categories. Outcomes included macroalbuminuria (>300 mg/24 h) or stage III chronic kidney disease (CKD) (sustained estimated glomerular filtration rate <60 mL/min/1.73 m2).ResultsDuring a median follow-up time of 24 years, there were 84 cases of stage III CKD and 169 cases of macroalbuminuria. In adjusted models, SBP in the <120 mmHg range was associated with a 0.59 times higher risk of macroalbuminuria (95% CI 0.37-0.95) and a 0.32 times higher risk of stage III CKD (95% CI 0.14-0.75) compared with SBPs between 130 and 140 mmHg. DBP in the <70 mmHg range were associated with a 0.73 times higher risk of macroalbuminuria (95% CI 0.44-1.18) and a 0.47 times higher risk of stage III CKD (95% CI 0.21-1.05) compared with DBPs between 80 and 90 mmHg. No interaction was noted between BP and prior DCCT-assigned glycemic control strategy (all P > 0.05).ConclusionsA lower BP (<120/70 mmHg) was associated with a substantially lower risk of adverse renal outcomes, regardless of the prior assigned glycemic control strategy. Interventional trials may be useful to help determine whether the currently recommended BP target of 140/90 mmHg may be too high for optimal renal protection in type 1 diabetes

Recombinant Vgr-1/BMP-6-expressing tumors induce fibrosis and endochondral bone formation in vivo.

Members of the TGF-beta superfamily appear to modulate mesenchymal differentiation, including the processes of cartilage and bone formation. Nothing is yet known about the function of the TGF-beta-related factor vgr-1, also called bone morphogenetic protein-6 (BMP-6), and only limited studies have been conducted on the most closely related factors BMP-5, osteogenic protein-1 (OP-1) or BMP-7, and OP-2. Because vgr-1 mRNA has been localized in hypertrophic cartilage, this factor may play a vital role in endochondral bone formation. We developed antibodies to vgr-1, and documented that vgr-1 protein was expressed in hypertrophic cartilage of mice. To further characterize the role of this protein in bone differentiation, we generated CHO cells that overexpressed recombinant murine vgr-1 protein. Western blot analysis documented that recombinant vgr-1 protein was secreted into the media and was proteolytically processed to yield the mature vgr-1 molecule. To assess the biological activity of recombinant vgr-1 in vivo, we introduced the vgr-1-expressing CHO cells directly into the subcutaneous tissue of athymic nude mice. CHO-vgr-1 cells produced localized tumors, and the continuous secretion of vgr-1 resulted in tumors with a strikingly different gross and histological appearance as compared to the parental CHO cells. The tumors of control CHO cells were hemorrhagic, necrotic, and friable, whereas the CHO-vgr-1 tumors were dense, firm, and fibrotic. In contrast with control CHO tumors, the nests of CHO-vgr-1 tumor cells were surrounded by extensive connective tissue, which contained large regions of cartilage and bone. Further analysis indicated that secretion of vgr-1 from the transfected CHO tumor cells induced the surrounding host mesenchymal cells to develop along the endochondral bone pathway. These findings suggest that endochondral bone formation

A new familial form of a late-onset, persistent hyperinsulinemic hypoglycemia of infancy caused by a novel mutation in KCNJ11.

The ATP-sensitive potassium channel (KATP) functions as a metabo-electric transducer in regulating insulin secretion from pancreatic β-cells. The pancreatic KATP channel is composed of a pore-forming inwardly-rectifying potassium channel, Kir6.2, and a regulatory subunit, sulphonylurea receptor 1 (SUR1). Loss-of-function mutations in either subunit often lead to the development of persistent hyperinsulinemic hypoglycemia of infancy (PHHI). PHHI is a rare genetic disease and most patients present with immediate onset within the first few days after birth. In this study, we report an unusual form of PHHI, in which the index patient developed hyperinsulinemic hypoglycemia after 1 year of age. The patient failed to respond to routine medication for PHHI and underwent a complete pancreatectomy. Genotyping of the index patient and his immediate family members showed that the patient and other family members with hypoglycemic episodes carried a heterozygous novel mutation in KCNJ11 (C83T), which encodes Kir6.2 (A28V). Electrophysiological and cell biological experiments revealed that A28V hKir6.2 is a dominant-negative, loss-of-function mutation and that KATP channels carrying this mutation failed to reach the cell surface. De novo protein structure prediction indicated that this A28V mutation reoriented the ER retention motif located at the C-terminal of the hKir6.2, and this result may explain the trafficking defect caused by this point mutation. Our study is the first report of a novel form of late-onset PHHI that is caused by a dominant mutation in KCNJ11 and exhibits a defect in proper surface expression of Kir6.2

Modeling and simulation of Li-Ion conduction in POLY(Ethylene Oxide

Prof. Moshe Israeli passed away on Feburary 18, 2007. This paper is dedicated to his memory Polyethylene oxide (PEO) containing a lithium salt (e.g. LiI) serves as a solid polymer electrolyte (SPE) in thin-film batteries and its ionic conductivity is a key parameter of their performance. We model and simulate Li + ion conduction in a single PEO molecule. Our simplified stochastic model of ionic motion is based on an analogy between protein channels of biological membranes that conduct Na +, K +, and other ions, and the PEO helical chain that conducts Li + ions. In contrast with protein channels and salt solutions, the PEO is both the channel and the solvent for the lithium salt (e.g., LiI). The mobile ions are treated as charged spherical Brownian particles. We simulate Smoluchowski dynamics in channels with a radius of ca 0.1nm and study the effect of stretching and temperature on ion conductivity. We assume that each helix (molecule) forms a random angle with the axis between these electrodes and the polymeric film is composed of many uniformly distributed oriented boxes that include molecules with the same direction. We further assume that mechanical stretching aligns the molecular structures in each box along the axis of stretching (intra-box alignment). Our model thus predicts the PEO conductivity as a function of the stretching, the salt concentration and the temperature. The computed enhancement of the ionic conductivity in the stretch direction is in good agreement with experimental results. The simulation results are also in qualitative agreement with recent theoretical and experimental results.

Prevention and treatment of bronchopneumonia in mice caused by mouse-adapted variant of avian H5N2 influenza A virus using monoclonal antibody against conserved epitope in the HA stem region.

The effects of monoclonal antibody (MAb) C179 recognizing a conformational epitope in the middle of the hemagglutinine (HA) stem region were examined in a mouse model in the experiments of prevention and treatment of lethal bronchopneumonia caused by influenza A virus of H5 subtype. To model the lethal infection, avian nonpathogenic strain A/mallard duck/Pennsylvania/ 10218/84 (H5N2) was adapted to mice. This resulted in highly pathogenic pneumovirulent mouse-adapted (MA) variant, which was characterized.